Study of QRS duration and R/Q Ratio in the Assessment of Severity of Acute Myocardial Infarction

A Dissertation on

STUDY OF QRS DURATION AND R/Q RATIO IN THE ASSESSMENT OF SEVERITY OF ACUTE MYOCARDIAL INFARCTION

submitted to

THE TAMILNADU DR. M.G.R. MEDICAL UNIVERSITY

CHENNAI

in fulfillment of the regulations

For the Award of the Degree of

M.D. (GENERAL MEDICINE)

BRANCH - I

KILPAUK MEDICAL COLLEGE

CHENNAI.

CERTIFICATE

This is to certify that “

STUDY OF QRS DURATION AND R/Q RATIO IN

THE ASSESSMENT OF SEVERITY OF ACUTE MYOCARDIAL

INFARCTION

” is bonafide work done by

Dr. SHYAM PADMANABHAN

,

postgraduate student, Department of

Internal Medicine

,

Kilpauk Medical

College

, Chennai-10 under my guidance and supervision in fulfillment of

regulations of The Tamilnadu

Dr. M.G.R. Medical University

for the award of

M.D. Degree Branch I, Part II (General Medicine)

during the academic period

from March 2005 to March 2008.

Dr. M. Dhanapal, M.D.,D. M.

The Dean

Kilpauk Medical College

Chennai 600 010

Prof. G. Rajendran, M.D.

Professor and Head

I thank

Dr. M. Dhanapal, M.D., D. M.,

Dean, Kilpauk Medical College for

permitting to use the resources and clinical material of this hospital.

I thank

Dr. G. Rajendran, M. D.,

Professor and Head of the Department of

Internal Medicine for granting me permission to conduct this study.

I thank

Dr. Narayanaswamy Senguttuvan, M. D., D. M.,

Professor and

Head of the Department of Cardiology for his valuable guidance and

encouragement.

I am grateful to

Dr. Surendran E

.

M.D

.,

Dr. Sundaramoothy. M.D.

,

Dr.

Jayaprakash. M.D.

,

Dr. Manickam. M.D.

, Assistant Professors in the ICCU for

providing immense help for the successful completion of this study.

I am grateful to

Dr. Mayilvahanan.S. M.D.,

Dr. Rohini I. M.D.,

Dr.

Vasanthi.P. M.D.

for their encouragement, guidance and support during the

course of the study.

I thank

Mr. Gopinathan.S.

for his valuable time spent in analyzing the data

and providing statistical support.

I also thank my fellow Post Graduate students and house surgeons for all the

CONTENTS

Chapter No.

Titles Page

No.

1 Introduction

2.

Aim and Objectives

3

Review of Literature

4

Materials and methods

5 Observations

6 Discussion

7 Conclusions

8

Appendix

Bibliography

Proforma

INTRODUCTION

Within a short span of time, Ischaemic Heart Disease (IHD) will be the number

one killer replacing infections, silently, slowly sometimes suddenly occluding the

coronaries of millions of Indians. WHO study group on IHD and atherosclerosis

described ischaemic heart disease as “cardiac disability, arising from reduction or arrest

of blood supply to the myocardium in association with disease process in coronary

arterial system.” During the past 30 years, a large decline in mortality due to coronary

artery disease has been experienced in the West and there is a substantial increase in the

developing countries. IHD accounted for 15.3 million deaths in 1996 which included

45.6% of all deaths in developed countries and 24.5% of all deaths in the developing

countries. Estimated and projected rates of death (per l,00,000) due to this dreaded

disease by World Bank Health Sectoral Priorities Review are 295 and 239 for males and

females respectively in the year 2015.

Coronary artery disease has a multifactorial etiology with many of the risk factors

being influenced by life style. Rapid change in dietary habits coupled with decreased

physical activity in India as a consequence of urbanisation may partly explain the

escalation of coronary artery disease. India is at going through a phase of rapid

urbanization which has led to economic improvement, the consequence of which has

resulted in fast food intake and tobacco consumption and decreased physical activity.

Atherosclerosis, which is the main cause of coronary artery disease is the

the precise cause of atherosclerosis is unclear an emerging paradigm suggests that

atherosclerosis involves multiple pathways in which lipoprotein entry and retention,

injury to vessel wall from diverse stimuli and an associated long term inflammatory and

immune response.

The standard 12 lead ECG has long been a reliable clinical tool for diagnosis of

myocardial infarction. Minutes may be crucial in making the decision for urgent

interventions in order to salvage the severely ischaemic myocardium. Besides history and

physical findings the ECG may be the only clinical tool available readily in deciding to

initiate life saving thrombolysis.

Identification of post infarction patients at risk for cardiac death and sudden

cardiac death may lead to optimization of medical therapy and implantation of

cardioverter-defibrillators. In the current era of technological development in cardiology

there are a number of methods that could be utilised for the risk stratification purposes.

Historically left ventricular ejection fraction was the first widely accepted risk stratifier in

post infarction patients. Subsequently interest in Holter recorded ventricular arrhythmias,

late potentials on signal averaged ECG, heart rate variability, substantiated prognostic

value of these parameters in patients with prior myocardial infarction. New approaches,

inc1uding heart rate turbulence, T wave alternans, QT variability and baroreflex

sensitivity are being successfully tried for risk stratification purposes. Simultaneous1y

invasive electrophysiology testing with induction of ventricular tachycardia or fibrillation

has been utilized for risk stratification purposes. The concrete evidence for dire

usefulness will known after extensive trials. All the above methods are worth exploring

general access to the technology and methodology needed to implement some of these

more sophisticated technique and also there are no standardizations of several of these

methods. A standard 12 lead ECG is widely, easily available and serves as a powerful

tool when considering risk stratification in post infarction patients. So a standard 12 lead

ECG is a cost effective excellent tool for estimating the severity of myocardial infarction

AIMS AND OBJECTIVES

1. To study the “QRS duration” on short term prognosis of acute myocardial

infarction.

2. To study the QRS duration in relation to 10-day hospital mortality.

3. To study R/Q ratio in lead II for the assessment of the severity of acute inferior

wall myocardial infarction.

4. To study the R/Q ratio in lead II in relation to thrombolytic therapy in acute

inferior wall myocardial infarction.

5. To study the comparison of R/Q ratio with QRS duration to assess the severity of

REVIEW OF LITERATURE

At the threshold of the new millennium coronary artery disease is looming large

as the new epidemic, afflicting Indians with severe and diffuse form of lesions. The

prevalence of coronary artery disease increased in India during the latter half of the last

century particularly among the urban population. (1)

The risk of coronary artery disease in Indians is 3 times higher than white

Americans, 6 times higher than Chinese and 20 times higher than Japanese. Indians are

prone as a community to coronary artery disease at a much younger age. (2)

In a metaanalysis Gupta and Gupta (1996) (3) estimated the prevalence of

coronary artery disease among Indians to be 9.6% in the urban and 3.7% in the rural

population. South Indians have a higher prevalence and 14 % in urban areas.

On screening persons over the age of 30 years by a 12 lead ECG in Chandigarh

the prevalence was found to be 65.4 and 47.8 per 1000 males and females respectively. In

a village of Haryana the prevalence was 22.8 and 17.3 per 1000 males and females

respectively .(4)

Although the death rate from acute myocardial infarction has declined by about

30% over the last decade, it is seen as a fatal event at the onset itself is seen in

approximately one third of patients. About 50% of the deaths associated with acute

myocardial infarction occur within 1 hour of the event and are attributed to serious

Almost all myocardial infarction results from coronary atherosclerosis, generally

with superimposed coronary thrombosis, slowly forming high grade stenosis in epicardial

coronaries may progress to complete occlusion, but yet does not usually precipitate acute

myocardial infarction, probably because of the development of a rich collateral network

over time. (6)

PATHOPHYSIOLOGY

On interruption of antegrade flow in an epicardial coronary artery, the zone of

myocardium supplied by that vessel immediately losses its ability to shorten and perform

contractile work (7), Four abnormal contraction patterns develop in sequences

a. Dyssynchrony - Dissociation in the time course of contraction of adjacent

segments.

b. Hypokinesis - Reduction in the extent of shortening.

c. Akinesis - Cessation of shortening.

d. Dyskinesis - Paradoxical expansion and systolic bulging.

Accompanying the dysfunction of the bulging segment, initially there is

hyperkinesis of the remaining normal myocardium. This increased motion subsides

within 2 weeks of infarction, during which time, some recovery can be seen in the infarct

region as well. Patients with acute myocardial infarction also show reduced myocardial

Clinical features: Chest pain and chest discomfort, are the predominant presenting

features of myocardial infarction. Nausea, vomiting and epigastric discomfort,

stimulating an abdominal pathology, occurs more commonly in patients with IWMI than

AWMI. The stimulation of vagus nerve or Bezold-Jarisch reflex is presumed to be the

mechanism involved. In elderly patients and diabetics, acute myocardial infarction can

manifest clinically without chest pain, but with symptoms of acute LVF and chest

tightness, or by marked weakness, or syncope. (9) Patients usually appear anxious and in

considerable distress. Sinus bradycardia is particularly frequent in, patients with inferior

and posterior wall infarction. (10) Hypotension, engorged neck veins, clear lung fields

and heart blocks are characteristic features of right ventricular myocardial infarction,

which occurs in about one-third cases of IWMI. (11)

On cardiac auscultation a fourth heart sound is almost always present in, patients

with acute myocardial infarction in sinus rhythm and this is usually best heard between

the left sternal border and the apex. In cases of RVMI associated with papillary muscle

dysfunction of the tricuspid valve, murmur of TR may be present. (7) In, patients with

IWMI, posterior involvement are associated with development of significant MR (12).

The incidence of cardiogenic shock and severe LVF occurs less frequently in

IWMI, unless otherwise, it is complicated by mechanical defects such as ventricular

Cardiac Enzymes

Estimation of the rise and fall in serum cardiac markers is one of the WHO

criteria for diagnosis of AMI, other being history of ischemia and electrocardiographic

changes. (13).

In myocardial infarction, as myocytes become necrotic, the integrity of the

sarcolemmal membrane is compromised and intracellular macromolecules (serum cardiac

markers) begin to diffuse into the cardiac interstitium and ultimately into the

microvasculature and lymphatics in the region of infarcts. (14) The rate of appearance of

these macromolecules depends on several factors including intracellular location,

molecular weight, local blood supply and lymphatic flow, and the rate of elimination

from the blood. (15).

Among the various serum cardiac markers; cardiac specific troponin (Tn-c, Tn-I),

Creatinine kinase (CPK-MB), Myoglobin and LDH are the commonly measured, with

troponin now considered as the preferred biomarker for diagnosis of acute myocardial

infarction (16). Serum level of cardiac enzymes appears to be the most practical means of

estimating infarct size (17). In addition, cardiac troponin measurements have been shown

to have prognostic value for identifying patients with an acute coronary syndrome at risk

for adverse clinical outcomes and who also exhibit enhanced responsiveness to new

therapies such as glycoprotein IIb/IIIa inhibitors and low molecular weight heparin (18).

Studies have shown that patients with IWMI who have anterior ST segment

depression and RVMI, have got higher cardiac enzyme values, indicating a larger mass of

ELECTROCARDIOGRAPHY

The value of ECG in diagnosing and localizing the size of infarction is

unequivocal. (20) The 12 lead ECG remains the centre of decision pathway for

management of patients with acute coronary syndrome and to distinguish between the

presentations of those with and without ST segment elevation (21). Katz et al (1946)(22)

set the criteria for electrocardiographic diagnosis of myocardial infarction. Myocardial

infarction was classified into transmural and non-transmural. Transmural were those

demonstrating significant Q wave plus typical ST-T wave alteration and T wave

inversion. In non-transmural infarcts, the established ST segment alteration and T wave

inversion persisted beyond 7 days, but with no significant Q waves.

The inferior wall of the left ventricle is directed to the standard leads II, III and

aVF (23). The hyperacute phase is manifested by increased ventricular activation time,

increased amplitude of R wave, straightening and subsequent slope elevation of the ST

segment, tall and widened T waves.

In the fully evolved phase, standard lead III commonly reflects a QS complex,

while standard lead II and aVF however usually reflect a QR complex. The disappearance

of the small normal initial Q in lateral leads is a corroborative sign of IWMI. Reciprocal

ST segment depression usually occurs in the right precordial leads. (24)

Q waves are frequently seen in lead III in normal patients, so to enhance the

specificity of Q wave in lead III, guidelines have been laid down. According to Harpaz D

et al (1999) (25), Q wave should he greater than 0.03 seconds. To increase the specificity

• Q in Lead II greater than 0.0 3second.

• Lead III Q greater than 0.03sec and Q greater than or equal to 1mm in

lead aVF.

• Lead aVF, Q greater than 0.03 see.

Along with IWMI, changes in the lateral leads (l, aVL, V5, V6) with an

isoelectric or elevated ST segment in lead I identifies obstruction of the circumflex

coronary arteries with a sensitivity specificity and predictive value of 83%, 96% and

93% respectively. Changes in lateral leads are rare in IWMI resulting from obstruction of

the RCA. (27)

ECHOCARDIOGRAPHY

Evaluation of LV Function:

The parameters of systolic and diastolic function can be obtained by M mode or

2D echocardiography, either by measuring left ventricular dimension in systole and

diastole or with LV volumes calculated by area length method in apical2D view.

Systolic Function: The three commonly used indices of systolic LV function are

LV Ejection Fraction = (EDV - E3V / EDV) X 100

Normal- in male 59±6 and in female 58±7

Fractional Shortening (FS) = (LVIDd - LVIDs / LVIDd) X 100

Normal - > 24 %

E-Point Septal Separation (EPSS)

Diastolic Function: The function is assessed by Doppler echocardiography by

calculating several indices but those in common use include peak ‘E’ velocity, peak ‘A’

velocity, E/A ratio and isovolumeic relaxation time. (28)

Segmental Wall Motion Analysis

The American Society of Echocardiography Committee (ASE) on Standards

recommended a semi-quantitative method that derives wall motion score based on a

visual impression of regional wall motion. The left ventricular mass can be divided into 3

equal levels from the apex to base length, resulting in its partition into basal, middle and

apical levels. They proposed a 16-segment model for visual semi-quantitative wall

motion analysis. (29)

The proposed segments are

Base Mid Apical

Basal Anterior Anterior Anterior

Basal Anteroseptal Anteroseptal Inferior

Basal lnferioseptal Inferioseptal Lateral

Basal Inferior Inferior Septal

Basal Posterior Posterior

The five basic wall region visualized are

Anterior Wall: Which was considered to extend over the anterior surface of

ventricles from the anterior interventricular sulcus, around the free ventricular wall to the

origin of the anterior papillary muscle.

Posterolateral wall: was considered to extend posteriorly between the papillary

muscles.

Inferior wall: Extended from the posterior papillary muscle to the junction with

the septum at the posterior interventricular sulcus.

Septal Region: Included the septum.

Apical Region: Included the very tip of ventricular cavity and apex.

One can relate the various segments to coronary artery distribution

Anterior and anteroseptal segments in both basal and middle third and the apical

segments - left anterior descending artery distribution.

Basal, lateral and middle lateral - left circumflex artery distribution.

Posterior and inferoseptal in both the basal and middle third - right coronary

artery distribution.

Scoring Scale: Henry et al (1979) (30) stated that at least 50% of the

endocardium must be visualized in anyone segment throughout the cardiac cycle for

reliable prediction of presence or absence of LV and RV asynergy. A significant concern

motion. For this, strict attention was paid not only to the endocardial inward motion but

also to the wall thickening. Liberman et al (1981) (31), showed that systolic thickening

provided better separation of normal from infarcted myocardium than endocardial motion

alone.

The ASE committee has also proposed the following scoring scale for

standardization of wall segment motion

Score Wall Motion Definition

1. Normal Normal endocardial inward motion and wall thickening in

systole

2. Hypokinesis Reduced endocardial motion and wall thickenil1g in systole

3. Akinesis Absence of endocardial inward motion or wall thickening in

systole

4. Dyskinesis Outward motion or bulging of the segment in systole, usually

associated with thin, scarred myocardium.

Wall Motion Score Index: It can be derived from the sum of all scores divided by

the number of segments visualized. (32).

Assessment of Overall Performance of the Ischemic Left Ventricle:

Left ventricular ejection fraction (LVEF) is one of the most commonly used

indices of systolic LV function. 2DE is a useful noninvasive method for estimation of LV

Following myocardial infarction, there is a decrease in LVEF and this is directly

related to the amount of damaged myocardium and the extent of potentially ischemic

muscle. Morbidity and mortality rates correlated well with initial ejection fraction.

Patients with ejection fraction <30-35% had greater risk of pump failure and death.

Patients with AWMI had a lesser LVEF (38±14) as compared to those with

inferoposterior wall myocardial infarction (55±10) because a greater region of

myocardium was involved in AWMI. (33).

In patients with IWMI, both LVEF and RVEF are depressed, whereas in patients

with AWMI, RVEF generally remains normal. But while RV performance rapidly

improves with prompt return to normal level, as early as 2 days after infarction, there is

less improvement in the LVEF. (34)

Carr et al (1979) (35) in their study found that cross-sectional echocardiography

and radionudeotide angiography were of equal value in the estimation of LVEF.

Although radionuc1eotide ventriculography generally provides a more exact

measurement of ejection fraction, echocardiography appears to be capable of directly or

subjectively evaluating ventricular function well enough to identify patients with risk of

COMPLICATIONS OF ACUTE MYOCARDIAL INFARCTION

Mechanical Complications:

1. Left Ventricular Failure: Even in thrombolytic era, left ventricular dysfunction

remains the single most important predictor of mortality after acute myocardial

infarction. In patients with acute myocardial infarction, heart failure is characterized

either by systolic dysfunction alone or by both systolic and diastolic dysfunction. Left

ventricular diastolic dysfunction leads to pulmonary venous hypertension and pulmonary

congestion whereas systolic dysfunction is principally responsible for a depression of

cardiac Output and of the ejection fraction. Clinical manifestations of left ventricular

failure become more common as the extent of the injury to the left ventricle increases;

mortality increases in association with the severity of the hemodynamic deficit.

Hemodynamic Classification of Patients with Acute Myocardial Infarction: (Killip

Classification)

Class Based on Clinical Examination Based on Invasive Monitoring

I No evidence of pulmonary congestion Normal

II Mild evidence of pulmonary congestion Pulmonary congestion PCWP > 18

CI<2.2

III Pulmonary oedema Peripheral Hypoperfusion

PCWP>18 CI>2.2

IV Cardiogenic Shock Pulmonary congestion and peripheral

2. Cardiogenic Shock: The severest clinical expression of left ventricular failure is

associated with extensive damage to the LV myocardium (about 40%) in more than 80%

of acute myocardial infarction patients in whom it occurs. The remainder have a

mechanical defects such as ventricular septal defect or papillary muscle rupture or

predominant right ventricular infarction. In the part cardiogenic shock has been reported

to occur in upto 20% of parents with acute myocardial infarction, but estimates from

recent large randomised trials of thrombolytic therapy and observational databases report

an incidence rate in the range 7% About 10% of patients with cardiogenic shock present

with this condition at the time of admission, whereas 90% develop it during

hospitalisation (36). Patients with cardiogenic shock due to acute myocardial infarction

are more likely to be older to have a history of a prior myocardial infarction or congestive

heart failure and to have sustained an anterior infarction at the time of development of

shock.

Arrhythmias:

Electrical instability: VPC’s, VT, VF, AIVR, NPAVJT

Pump failure/ excessive sympathetic stimulation: Sinus tachycardia AF / Afl, PSVT

Bradyarrhythmias and conduction disturbances

Progression of Acute Myocardial Infarction: Most of the thrombolytic trial shows that

mortality in IWMI is about half that of AWMI.

Name of Studies

AWMI IWMI

No. of Deaths

No. of

Patients %

No. of Deaths

No. of

Patients %

GISSI-I 403 2193 18.4 145 2004 7.2

ISIS 329 1827 18.0 185 2112 8.8

AIMS 51 292 17.5 26 225 7.8

ASSRT 134 796 16.8 77 773 10.0

LATE 58 410 14.2 30 351 8.6

Average - 16.98% Average – 8.48%

Certain high risk subgroups can be identified in IWMI by single ECG criteria.

These are right precordial ST segment elevation, left precordial ST segment depression

and high degree AV block. 2D echo can also diagnose high risk subgroups like those

having RV and posterior wall assynergy, patients having poor ejection fraction, high wall

motion index score, VSD, papillary muscle ruptures etc. These high risk subgroups have

similar mortality rates as of AWMI, while the low risk subgroups have got mortality rates

The results of thrombolytic trials in myocardial infarction show that thrombolysis

in IWMI is statistically not as significant as in anterior wall myocardial infarction and it

has got only a meager impact in the mortality reduction.

Studies Thrombolytic Deaths/ Patients

Control Deaths/ Patients

Streptokinase

GISSI-I (0-12 h) 137/2009 (6.8%) 145/2004 (7.2%)

ISIS-2 (0-24h) 150/2076 (7.2%) 185/2112 (8.8%)

SK/ASA ISIS-2 (0-24h) 69/1016 (6.8%) 107/1047 (10.2%)

Altepase

ASSET (0-5h) 46/734 (6.3%) 77/773 (10.0%)

LATE (6-12h) 34/381 (8.9%) 30/351 (8.6%)

Prognostic Significance of ECG in Acute Myocardial Infarction

Standard 12 lead ECG serves as an extremely useful tool in risk stratification after

myocardial infarction. Careful analysis of ECG provides comprehensive information

about pathology of the heart, which could lead to cardiac events including reinfarction,

progression of heart failure and death. Identification of post infarction patients at risk or

cardiac death and sudden cardiac death may lead to optimization of medical therapy and

implantation of cardioverter defibillators.

QRS Duration and Myocardial Infarction

In a study by Pudil et al (2001) (38), acute myocardial infarction with

intermediate QRS duration (0.09-0.11sec) on admission electrocardiogram was

More recently it was shown that QRS duration of the admission

electrocardiogram is independently associated with 30 days and 1 year mortality after

acute myocardial infarction in the GUSTO-1 trial. In this trial QRS prolongation had a

more significant outcome in patients with anterior myocardial infarction (39).

Prolonged QRS duration on surface electrocardiogram was associated with left

ventricular dysfunction in patients referred to radionucleotide exercise ventriculography.

It was also reported that QRS (duration > 0.1 seconds indicated decreased left ventricular

ejection fraction .(40).

A QRS of < 0.09 seconds on admission electrocardiogram is indicate of a relative

benign outcome compared with a QRS duration of >0.09 seconds.

The mechanism by which prolonged QRS duration on admission is associated

with increased risk of death is not clear. Multiple physiologic parameters associated with

poor outcome can lead to prolonged QRS duration in patients with acute myocardial

infarction including increased left ventricular muscle mass, myocardial fibrosis, increased

area of necrosis, involvement of conduction system in the ischaemic area, poor metabolic

state that slows conduction, and effects of various medications.

After adjusting for all significant variables associated with mortality, including

age, gender, diabetes mellitus, smoking, systemic hypertension, Killip class>2 on

admission and anterior location of myocardial infarction prolonged QRS duration both in

the those with QRS duration> 0.11 seconds was found to be independently associated

QRS prolongation was positively associated with older age, female gender,

anterior myocardial infarction and congestive heart failure on admission.

In 743 patients of the placebo arm of the cardiac arrhythmia suppression trial

1991 with stable coronary artery disease and QRS duration >100 ms, the risk ratio was

1.4 for new or worsening congestive heart failure, 1.5 for arrhythmic death or cardiac

arrest and 1.4 for all cause mortality (p<.05). In post acute myocardial infarction patients

QRS prolongation was significantly correlated with arrhythmic events (41).

In patients with normal coronary arteries, QRS duration decreases with exercise

probably because of an increase in the sympathetic tone. In contrast, in patients with

coronary artery disease, QRS duration increases during exercise testing. Michaelids et al,

1993(42) reported that exercise induced QRS prolongation was proportional to the

number of coronary arteries with >70% stenosis. Mean QRS prolongation was 4.8±7.5

ms in patients with I-vessel disease, 7.8±11.8 ms in patients with 2-vessel disease and

13.3±12.1 ms in patients with 3-vessel disease (p< 0.001).

Distortion of the terminal portion of the QRS complex in the admission ECG is an

independent predictor of increased hospital mortality in patients receiving thrombolytic

therapy >2 hour after the onset of symptoms. During regional myocardial ischemia the

conduction velocity of the activation wave in the Purkinje fibres is prolonged .(43)

QRS prolongation on surface electrocardiography has been identified as a marker

for increased cardiac mortality. A potential mechanism for increased mortality is

ventricular tachycardia. Patients with prolonged QRS duration were older had lower

was a significant predictor of sustained monomorphic VT inducibility (p< 0.0001). On

Multivariate analysis correcting for age, sex, LVEF, history of myocardial infarction,

medication and QRS conduction delay proved to be independently associated with

sustained monomorphic VT inducibility (relative risk 3.290, 95% confidence interval

2.185 to 4.953 for prolonged vs. normal QRS duration) (44).

At multivariate analysis, prolonged filtered QRS duration had an independent

relation to late arrhythmic events after acute myocardial infarction. (45)

QRS duration remains a very powerful predictor of future cardiac events in post

infarction patients (46). QRS duration reflects well the magnitude of left ventricular

dysfunction and therefore not surprisingly is a powerful predictor of mortality in post

infarction patients.(40). A study by Fadl et al (2003) (47) in a large population of post

infarction patients indicate that QRS duration 0.12 second is associated with hazard ratio

of 1.7; p = 0.001.

Significance of R/Q Ratio in Lead II in Inferior Wall Myocardial Infarction

Inferior wall of the heart is constituted by the inferior wall of left ventricle and is

oriented to the positive electrodes of lead II, III, avF.

Inferior wall myocardial infarction has 3 phases

1. Early hyper acute - characterized by elevation of ST segments.

2. Ful1y evolved phase - characterized by the presence of pathological Q or QS

complexes coved and elevated ST segments and inverted sharply pointed and

3. Chronic stabilized phase - Characterized by residual Q wave abnormalities in

leads II, III, avF, particularly in lead II, avF.

Pathological Q waves of inferior wall myocardial infarction are not usually deep

or as wide as the pathological Q waves which occur with anterior wall myocardial

infarction because inferior wall myocardial infarction is reflected by extremity leads (48).

In IWMI a QS complex is usually present in lead III and avF. Standard lead II

usually reflects Qr or QR complex. In inferior wall myocardial infarction, among the

inferior leads tallest terminal R wave is seen in lead II. (48)

We can explain this distribution of terminal R wave by considering the anatomy

of inferior wall. We can divide the inferior wall into right lateral and left lateral region.

Lead III is oriented to right lateral region and lead II to left lateral region.

The brunt of infarction affects the right lateral region of inferior wall with sparing

of left lateral region so lead III reflects the largest and widest QS complex, lead II

however is oriented to left lateral region of inferior wall reflects the potentials of healthy

overlying muscle as a terminal R wave; so loss of R wave in lead occurs mainly in

Two major determinants of clinical outcome in patients with acute myocardial

infarction are the extent of infarction and the residual left ventricular function (49).

In patients with inferior wall myocardial infarction terminal R wave and R/Q ratio

in lead II reflects the extent of infarction and residual function so by calculating R/Q ratio

Alexander Arditti et al (1985) (50) studied a simplified QRS scoring system for

the estimation of the severity of acute inferior myocardial infarction.

Electrocardiographic assessment of the R/Q ratio in lead II of patients with first acute

inferior wall myocardial infarction offers important indirect evidence of severity and

extent of myocardial infarction. An R/Q ratio of more than 2 predicts mild and localized

left ventricular involvement with good global left ventricular function and good clinical

course. An R/Q ratio between 1 and 2 predicts a greater degree of local asynergy with

some lateral extension with reduced global left ventricular function, but still a good

clinical outcome. R/Q ratio less than one predicts severe inferior wall asynergy with high

incidence of lateral wall involved, reduced global left ventricular function and

complicated clinical course during the acute phase.

Eliezer et al (1988) (51) conducted similar study in which acute inferior wall

myocardial infarction were divided into three groups according to the R/Q ratio in lead II.

This was done to correlate these groups with characteristic course to electrocardiographic

status. Patients with R/Q > 2 (group 1) had a more rapid progression through the

electrocardiographic stages along with better clinical course than patients with lower R/Q

ratio. Patients in group In with R/Q < 1 had a slower electrocardiographic stage

progression which correlates well with a more complicated clinical course. Group II was

an intermediate group in both the electrocardiographic and clinical course. It is suggested

that the R/Q ratio in lead II can be used as a marker of the severity of IWMI since it

correlates well with the course of electrocardiographic stages. This may be an additional,

simple and inexpensive electrocardiographic tool for following the natural course of

Lewin (1986) (52) conducted a study in which acute inferior wall myocardial

infarction were divided into three groups. Group I predominant right ventricular

infarction, group II combined right and left ventricular infarction and in group III

predominant left ventricular infarction. Patients with predominant RV infarction (Group

I) had smaller Q wave values and taller mean R wave in the inferior leads than patients in

the other groups. In predominant RV infarction R/Q ratio> 2.5 and is combined RV and

MATERIAL AND METHODS

The study was carried out on 75 patients admitted in ICCU of Department of

Medicine, Government Royapettah Hospital, Kilpauk Medical College, Chennai-10.

SELECTION CRITERIA:

In this study 75 cases of both sexes of more than 20 years of age with first episode

of myocardial infarction, typical chest pain of more than 30 minutes, onset of symptoms

within previous 6 hours, at least 0.2 mv ST segment elevation in two or more contiguous

precordial leads or at least 0.1mv ST segment elevation in two or more leads were

included.

The screening criteria for the identification of the presence of myocardial

infarction were:

• Inferior criterion: Q>30 msec in lead aVF

• Anterior criteria: A Q or R< 0.1 mv and < 10 m sec in V2.

EXCLUSION CRITERIA

Patients with ECGs showing evidence of LBBB, RBBB, LAHB, LVH, old

myocardial infarction, preexicitation syndrome were excluded from the present study.

All cases were subjected to following examination.

Case number, registration number, father/husband name, age, sex,

Presenting complaints with duration were noted in detail such as chest pain, its

site, duration and radiation, accompanying features like sweating, nausea, vomiting,

syncope, breathlessness, palpitation, oedema, abdominal distension, right hypochondrial

pain and other atypical symptoms.

Detailed symptomatology of clinical presentation was sought with special

reference to onset, duration, intensity, relationship to circadian and seasonal rhythm of

symptoms.

Past History

It was taken to exclude the presence of a previous myocardial infarction and to

find out the risk factors including hypertension, diabetes mellitus and other evidence of

atherosclerotic disease like CVA.

Family History

Family history of diabetes mellitus, coronary artery disease, hypertension,

dyslipidemia, age of death were enquired for.

Personal History

It was taken with special reference to addictions like tobacco chewing, smoking,

General Examination:

It was done meticulously in all cases, special care was taken to record pulse rate,

rhythm, volume, character and condition of arterial wall. Blood pressure was taken to

supine position. Presence of pallor, cyanosis, pedal oedema and raised JVP was noted.

Systemic Examination

• Detailed Cardiovascular system examination was done by observing,

palpating apex impulse, thrills, precordial pulsations were looked for, heart

sounds S1, S2, S3 and S4, murmurs were auscultated. (site, duration, timing,

character and radiation).

• Respiratory system was examined by auscultating for breath sounds and to

look for evidence of pulmonary oedema.

• Abdominal examination was done for the presence of any organomegaly and

ascites.

• Central nervous system was examined for presence of any neurological

deficit.

Investigations

The following investigations were done in all cases.

• Haemogram - Hb, TLC, DLC, ESR.

• Urine - Albumin, Sugar and Microscopy

Electrocardiogram:

12 lead ECG was taken in all cases taking special precautions while placing the

chest leads. Repeat ECGs were taken every day on first three consecutive days of

admission followed by every alternate day until 10th day.

Rigorous Definition of Wave Forms

When the initial aspect of the QRS complex is negative, a Q wave is present.

Prior to returning to the baseline, this negative deflection may be smooth or notched. A

smooth q wave is present when the initial negative deflection contains no reversal in the

direction of 0.05 mv or more.

The duration and amplitude of such Q wave are measured as the width and depth

respectively of the initial negative deflection.

A notched Q wave is present if there is a reversal in direction of 0.05 mv or more

within the initial negative deflection. In this instance, the duration of the Q wave should

be measured along the PR baseline only to the point directly above the peak of the notch

and remainder of the negative deflection should not be considered. The amplitude of the

Q should be measured to the nadir of the negative deflection preceding the notch.

An R wave is defined on the initial positive deflection. A notched R wave is

present if there is a reversal in direction of 0.05 mv or more within the initial 40 ms of the

Accurate Wave from Measurement:

Careful manual measurement of both amplitudes and duration should be made

with calipers using center of the trace of the inscribed waveform.

Rand Q wave amplitude and resultant R/Q ratio were calculated in lead-II using

and 7th day of hospitalisation. By using 3rd day R/Q ratio on lead-II short term prognosis

of inferior wall myocardial infarction was evaluated. By comparing R/Q ratio on 7th and

3rd day the relationship of thrombolysis and R/Q ratio was evaluated.

For the study, patients of inferior wall myocardial infarction were divided into

groups according to R/Q ratio in lead II on 3rd day.

Group I Includes patients of IWMI with R/Q ratio> 2

Group II Includes patients of IWMI with R/Q ratio 1- 2

Group III Includes patients of IWMI with R/Q ratio < 1

For the study of QRS duration, widest QRS duration in standard lead was

manually measured on 3rd day of hospitalisation.

Only leads without extreme ST segment deviation were considered. According to

the QRS duration, patients of myocardial infarction including both inferior and anterior

wall myocardial infarctions were divided into 3 groups.

Group A With QRS duration < 0.09 See.

Group B With QRS duration 0.09 - 0.11 sec (intermediate QRS

prolongation)

ECHOCARDIOGRAPHY

The 2 dimensional echocardiography study was performed on the 7th day post

myocardial infarction, with the patient in the left lateral decubitus position with Toshiba

Model SSH -140 echocardiography machine. A 3.75 MHz phased array sector transducer

was used. The left ventricle was studied as recommended by American Society of

Echocardiography in the long and short view.

The committee proposed the following scoring scale for standardization of wall

segment motion.

A normally contracting segment or a hypercontracting segment is assigned a score

of 1, Hypokinesia 2, Akinesia 3, Dyskinesia 4 and aneurysmal segment 5.

Dyssynergy of a LV segment was defined as Hypokinesis, Akinesis or Dyskinesis

involving> 50% of that segment.

The ejection fraction was calculated by the standard formula as recommended by

American Society of Echocardiography 1989(ASE).

Left Ventricular Ejection Fraction:

EDV -ESV

(LVEF) =--- X 100

EDV

EDV = End Diastolic volume

Normal> 60%

The QRS duration and R/Q ratio were evaluated with ejection fraction and

regional wall motion abnormalities.

Statistical Analysis

In present study comparison among the three groups using tables and graphic

presentations were performed. The analysis between groups was performed using student

‘t’ test or the Chi Square test when indicated. All data were expressed as mean standard

OBSERVATION

The present series “Study of QRS Duration and R/Q ratio in the assessment of

Severity of Acute Myocardial Infarction” was carried out on 75 patients admitted in

ICCU of Department of Medicine, Government Royapettah Hospital, Kilpauk Medical

College, Chennai-10.

Table No.1

Distribution of Type of Myocardial Infarction

S. No. Type of Myocardial Infarction No. of Cases Percentage

1. AWMI 28 37.33

2. IWMI 44 58.67

3. AWMI+ IWMI 3 4.0

Total 75 100.0

58.67% of the patients were having inferior wall myocardial infarction, 37.33% were

having anterior wall myocardial infarction while 4.0% patients had both anterior and

Table No. 2

Thrombolytic Therapy in Acute Myocardial Infarction

S. No Type of M.I.

Total Thrombolyzed Non Thrombolyzed

No. % No. % No. %

1. AWMI 28 37.33 14 50.0 14 50.0

2. IWMI 44 58.67 24 54.54 20 45.46

3. AWMI +IWMI 3 4.00 2 66.67 1 33.33

Total 75 100.0 40 53.33 35 46.67

X2 = 6.06, p <0.05 Significant

Out of total cases 53.3% patients were thrombolyzed.

Table No. 3

Distribution of Ejection Fraction

Type of Myocardial Infarction

< 40% 41-50 % > 50%

No. % No. % No. %

AWMI (n-26) 9 34.61 13 50.0 4 15.38

IWMI (n-41) 7 '17.07 21 51.21 13 31.70

AWMI +IWMI (n-3) 1 33.33 2 66.67 - -

Total (n-70) 17 24.28 36 51.42 17 24.28

X2 = 41.86, p <0.001 Highly Significant

Most of the patients with of anterior wall myocardial infarction had left

ventricular ejection fraction in the range of 41-50%. Nine patients (34.61%) with anterior

wall myocardial infarction had left ventricular ejection fraction < 40%, against 17.07%

patients of inferior wall myocardial infarction.

Table No. 4

Distribution of Myocardial Infarction in Relation to QRS Duration

ORS Duration (In Seconds)

IWMI AWMI Total

No. % No. %

Group A (<0.09) 32 65.30 17 34.69 49

Group B (0.09- 0.11) 9 50.0 9 50.0 18

Group C (>0.11) 6 75.0 2 25.0 8

Total 47 62.67 28 37.33 75

X2 = 13.70, p <0.05 Significant

65% of the patients with combined inferior wall myocardial infarction and

anterior wall myocardial infarction were distributed in group A (<0.09) 40% patients with

anterior wall myocardial infarction alone had QRS duration >0.09 seconds as compared

Table No. 5

QRS Duration and Cardiac Arrhythmias in Myocardial Infarction

Arrhythmia

Group A (< 0.09) (n-49)

Group B (0.09 – 0.11 ) (n-18)

Group C

(> 0.11) (n-8) Total

No. % No. % No. % No. %

S.V.E. 3 50.0 1 16.67 2 33.3 6 16.21

V.E. 12 66.67 4 22.22 2 11.11 1R 48.04

S.V.T. - - 2 10O.n - - 2 5.4

V.T. 3 33.33 4 44.44 2 22.22 9 25.0

C.H.B. - - 2 100.0 - - 2 5.4

Ventricular ectopics were the most common arrhythmia observed. Maximum

incidence of ventricular tachycardia was in group B (44.44%).

Table No. 6

QRS Duration and Regional Wall Motion Abnormality

Group A Group B Group C

RWMA (0.09) (0.09 - 0.11 ) (> 0.11) Total (n-69) (n-49) (n-18) (11-8)

No. % No. % No. % No. %

Hypokinesia 22 84.61 2 7.69 2 7.69 26 37.14

Akinesia 24 57.14 14 33.3 4 9.52 42 60.0

Normal 2 100.0 - - - - 2 2.86

Total 48 68.57 16 22.85 6 8.5 70* 100.0

84.61 57.14 7.69 33.3 7.699.52 0 10 20 30 40 50 60 70 80 90 Percentage

1 2 3

QRD Duration

QRS DURATION AND REGIONAL WALL M OTION ABNORM ALITY

Hypokinesia Akinesia

QRS DURATION AND EJECTION FRACTION

0 10 20 30 40 50 60 70 80 90 100

1 2 3

QRS Duration Pe rc e n ta g e

Akinesia was reported from 24 patients (50%) of group A, 14 patients

(87.5%) of group B and 4 patients (66.67%) of group C. Hypokinesia was reported

from 22 patients (46%) of group A, 2 patients (12.5%) of group B and 2 patients

(33.33%) of group C. Two patients in Group A were having normal regional wall

motion.

Table No. 7

QRS Duration and Ejection Fraction

Ejection Group A Group B Group C Total

« 0.09) (0.09 - 0.11) (> 0.11)

(n-70) Fraction (n-49) (n-18) (n-8)

(%)

No. % No. % No. % No. %

30-40 % 6 35.29 9 52.94 2 11.76 17 24.28

40-50 % 25 62.85 7 20.0 3 8.57 35 50.0

50-60 % 16 94.1 - - 1 5.9 17 24.28

> 60% 1 100.0 - - - - 1 1.42

Total 48 68.11 16 23.18 6 8.69 70* 100.0

*5 Patients expired before Echocardiography.

In Group A, patients with ejection fraction >50 was 35.45%. In Group C

patients with ejection fraction >50 was 16.7% and in Group B patients had ejection

Table No. 8

Killip Class and Distribution of Cases in Myocardial Infarction in Relation to QRS Duration

Killip Class A (n-49) B (n-18) C (n-8)

No. % No. % No. % No. %

I 35 71.4 5 27.78 1 12.5 41 54.67

II 12 24.48 10 55.55 2 25.0 24 32.0

5.5 50.0

III 1 2.0 1 4 6 8.0

IV 1 2.0 2 11.11 1 12.5 4 5.3

Total 49 65.33 18 24.0 8 10.67 75 100.0

Chi square=39.21 p< 0.001 Highly Significant (Gr A vs B) Chi square=104.88 p<0.001 Highly Significant (Gr A vs C) Chi square=53.15 p<0.001 Highly Significant (Gr B vs C)

In group A 71.4 % of patients belonged to Killip class I as compared to 12.5% in

group C. Patients with Killip class > II were62.5% in group C, 16.6% in group B and 4%

in group A.

Table No. 9

Killip Class with Mean QRS Duration and Ejection Fraction in AWMI

Killip Class Mean QRS Duration Mean Ejection Fraction

I 0.08±0.01 47.60±9.82

II 0.09±0.01 42.20±4.78

III 0.09 43

N 0.10 Expired before Echo

K IL L IP C L AS S AND DIS T R IB UTION OF C AS E S IN MYOC AR DIAL 

INF AR C T ION IN R E L ATION T O QR S DUR ATION  

0 10 20 30 40 50 60 70 80

G roup A (< 0.09) G roup B (0.09‐0.11) G roup C (>0.11)

QR S Duration

Pe rc e n ta g e

S eries 1 S eries 2 S eries 3 S eries 4

10 DAY MORTALITY IN DIFFERENT GROUPS IN

RELATION TO QRS DURATION

98 83.35 75 2 16.67 25 0 20 40 60 80 100 120

1 2 3

Mean QRS duration of class I patient was 0.08±0.01 as compared to 0.10 in

Killip class IV patients. As QRS duration increases Killips Class also increases.

Table No. 10

10 Day Mortality in Different Groups in Relation to QRS Duration

Survivors Expired Total

QRS Duration

No. % No. %

Group A (< 0.09) 48 98.0 I 2.0 49

Group B (0.09 - 0.11 ) 15 83.35 3 16.67 18

Group C(> 0.11) 6 75.0 2 25.0 8

Total 69 92.0 6 8.0 75

Chi square= 21.80 p< 0.001 Highly Significant

In the present study out of the 75 patients 6 (8.0%) expired; one from Group

A (2.0%)/ 3 from group B (16.67%) and 2 (25.0%) from group C. In the mortality

group, except one patient of AWMI, five of them expired before Echocardiography

Table No. 11

Distribution of IWMI According to R/Q Ratio in Lead II

S.No. R/Q Ratio in Lead II No. of Cases Percentage

1. Group I (> 2 ) 22 46.80

2. Group II (1-2 ) 21 44.68

3. Group III (< 1 ) 4 8.51

Total 47 100.0

Maximum number of patients were in group I (46.80%) followed by group II

(44.68%).

Table No. 12

R/Q Ratio and Complications at the Time of Admission

S. N. Complications R/Q Ratio

Group I (> 2) Group II (1-2) Group III (<1)

(n-22) (n-21) (n-4)

1. Hypotension - 1 (4.76%) 1 (25.0%)

2. Raised JVP 3 (13.63%) 4 (19.0%) 2 (50.0%)

3. Arrhythmia 7 (31.81 %) 9 (42.8%) 2 (50.0%)

Chi square= 22.91 p<0.001 Highly Significant.

All patients of group III had different types of complications of myocardial

infarction, 50% of them developed arrhythmia, 50% had raised JVP and 25% had

raised JVP and none of them had hypotension

Table No. 13 R/Q Ratio and Arrhythmia

Group I Group II Group III Total (n-17)

Arrhythmia (R/Q > 2) (R/Q 1-2) (R/Q < 1)

No. % No. % No. % No. %

S.V.E. 1 20.0 3 60.0 1 20.0 5 29.41

V.E. 4 57.14 3 42.85 - - 7 41.17

S.V.T. - - 1 100.0 - - I 5.88

V.T. 1 33.3 1 33.3 1 33.3 3 17.64

C.H.B. - - 1 100.0 - - 1 5.88

Most common arrhythmia reported was ventricular ectopics (41.1%) followed by

supraventricular ectopics (29.4%). Out of 47 patients with inferior wall myocardial

infarction only 3 patients (17.64%) had ventricular tachycardia, with 33.3% of patients in

each group.

Table No. 14

R/Q Ratio and Ejection Fraction in Thrombolyzed and Non Thrombolyzed in Inferior Wal1 Myocardial Infarction

S. N. IWMI (n-47) R/Q Ratio Ejection Fraction

(Mean±S.D.) (Mean±S.D.)

1. Thrombolyzed (n-26) 2.89±1.54 48.84±5.56

2. Non-thrombolized (n-21) 1.89±1.0 46.89±6.78

There is statistically significant difference in mean R/Q ratio and EF in

thrombolysed and non thrombolysed patients of inferior wall myocardial infarction.

Table No. 15

Relationship of Change in R/Q Ratio with Thrombolysis

Changes in R/Q Ratio Thrombolyzed Non-thrombolyzed

from 3rd to 7th Day (n-26) (n-21)

No. % No. %

Increase in R/ Q Ratio - - - -

No Change in R/Q Ratio 22 84.61 13 61.10

Decrease in R/Q Ratio 4 15.35 8 38.09

Chi square=9.92 p<0.05 Significant

Out of 26 patients of inferior wall myocardial infarction thrombolyzed 22

patients (84.61 %) had no change in R/Q ratio from 3rd day to 7th day. But 4 patients

(15.35%) showed a decrease in R/Q ratio on 7th day as compared to R/Q ratio on 3rd

day. In non-thrombolyzed patients of IWMI 8 patients (38.09%) showed a decrease in

R/Q ratio on 7th day as compared to R/Q ratio on 3rd day. So significantly less

number of patients showed decrease in R/Q ratio in thrombolyzed as compared to

RELATIONSHIP OF CHANGE IN R/Q RATIO WITH THROM BOLYSIS 84.61 61.1 15.35 38.09 0 10 20 30 40 50 60 70 80 90 1 2 P er cen ta g e

No Change in R/Q Ratio Decrease in R/Q Ratio

R/Q RATIO AND REGIONAL WALL M OTION ABNORM ALITIES (RWM A)

0 10 20 30 40 50 60 70 80

1 2 3

R/Q Ratio Pe rc e n ta g e

Table No. 16

R/Q Ratio and Regional Wall Motion Abnormalities (RWMA)

RWMA Group I Group II Group III

(>2) (1-2) «1)

No. % No. % No. %

Hypokinesia (n-22) 14 63.64 6 31.57 2 66.67

Akinesia (n-21) 7 31.8 13 68.43 1 33.3

Normal (n-1) 1 4.54 - - - -

Total (n-44) 22 100.0 19 100.0 3 100.0

*3 patients of IWMI expired befor Echocardiography.

Chi square=10.23 p<0.05 Significant (I vs III) Chi square=12.99 p<0.05 Significant (II vs III) Chi square=25.69 p<0.001 Highly Significant (I vs II)

Out of 22 patients in group I, 14patients (63.64%) had hypokinesia and 7 patients

(31.8%) had akinesia of inferior segment of left ventricle. Out of 44 patients of IWMI; 22

patients had hypokinesia in which 14 patients (63.64 %) belonging to group I; only 2

patients (9.0%) belonged to group III.

Table No. 17

R/Q Ratio in Lead II and Ejection Fraction in IWMI

S. No. RlQ Ration in Lead II No. of Cases Mean Ejection Fraction

1. Group I (> 2) 22 49.91±5.99

2. Group II (1-2) 21 46.10±5.84

3. Group III (< 1) 4 42±6.32

R/Q RATIO IN LEAD II AND EJECTION FRACTION IN IWMI (N-47) 38 40 42 44 46 48 50 52

1 2 3

R/Q Ratio in Lead II

Me a n E je c ti o n Fr a c ti on

KILLIP CLASS AND DISTRIBUTION OF CASES IN INFERIOR WALL M YOCARDIAL INFARCTION

17 4 1 0 12 6 3 0 3

0 0 1

0 2 4 6 8 10 12 14 16 18

1 2 3 4

Killip Class No . o f Ca s e s

Among the various groups, maximum mean ejection fraction was reported in

group I i.e. R/Q > 2. Lowest mean ejection fraction was in patients with R/Q ration < 1

(group III).

Table No. 18

Killip Class and Distribution of Cases in IWMI

Killip Group I Group II Group III

(R/Q> 2) (R/Q 1-2) (R/Q < 1) Class

No. % No. % No. %

I ( n=32) 17 77.2 12 57.0 3 75.0

II (n=10) 4 18.18 6 28.5 - -

III (n=4) 1 4.54 3 14.28 - -

IV (n=1) - - - - 1 25.0

Total 22 100.0 21 100.0 4 100.0

(n=47)

Chi square=70.23 p<0.001 Highly Significant (Gr I vs Gr III) Chi square=10.36 p<0.05 Significant(Gr I vs Gr II)

Out of 32 cases of Killip class 117 (53.12%) patients from Group I and 3 (9.37%)

patients are from group III. Only one case of Killip class IV was reported from the

present study, which was from group III. Majority of group II patients were in Killip

Table No. 19

Killip Class with Mean R/Q Ratio and Ejection Fraction in IWMI

Killip Class Mean R/Q Ratio Mean Ejection Fraction

I 2.66 ±1.49 49.55 ±5.22

II 2.19 ±1.02 46.64 ±6.61

III 2.0 ±1.73 40.0 ±5.29

IV 0 38

r =-1.0, insignificant r = -1.0, insignificant

Mean R/Q ratio of Killip class I was 2.66 ±1.49 against 2.0 ±l.73 in Killip class

III. Mean ejection fraction of Killip class I was 49.55 ±5.22 and 40.0 ±5.29 in Killip class

III. There was a weak correlation between mean R/Q ratio and mean ejection fraction

with Killip class.

Table No. 20

Comparison of R/Q Ratio and QRS Duration in Relationship to Ejection Fraction

S.No. R/Q Ratio Mean Ejection QRS Duration Mean Ejection

Fraction Fraction

1. Group I (> 2) 49.91 ±5.99 Group A (< 0.09) 48.96 ±6.53

2. Group II (1-2) 46.10 ±5.84 Group B (0.09 - 0.11 ) 40.94 ±3.90

3. Group III (<1) 42 ±6.32 Group C (> 0.11) 43.17 ±4.83

Mean ejection fraction of group I was 49.91 ±5.99 and group A

was 48.86 ±6.53. Mean ejection fraction of group III was 42 ±6.32 and in group C it

was 43.17 ±4.83, as R/Q decreases the reduction in mean ejection fraction was also

significant. Similar to this prolongation of QRS duration also correlates with

(0.09-0.11) in Group B had lowest mean ejection fraction.

Table No. 21

Correlation of R/Q Ratio Groups with QRS Duration Groups in IWMI

R/Q Ratio No .of QRS Duration No. of %

Patients Patients

Group A «0.09) 20 90.90

Group I

22 Group B (0.09-0.11) 2 9.10 (R/Q> 2)

Group C (>0.11) 0 0

Group A (>0.09) 11 52.4

Group II

21 Group B (0.09-0.11) 5 23.80 (R/Q 1- 2)

Group C (>0.11) 5 23.80

Group A (<0.09) 1 25.0

Group III

4 Group B (0.09-0.11) 2 50.0 (R/Q < 1)

Group C (>0.11) 1 25.0

Percentage of patients with QRS duration < 0.09 sec was 90.90% in group I,

52.40% in group II and 25% in group III.

In group III (R/Q<l) 25% patients belong to group A and 25% belong to group

QRS DURATION AND MEAN EJECTION FRACTION 48.96 40.94 43.17 36 38 40 42 44 46 48 50

1 2 3

QRS Dur ation

M e a n E je c ti on Fr a c ti on

CORRELATION OF R/Q RATIO GROUPS AND QRS DURATION GROUPS 0 10 20 30 40 50 60 70 80 90 100

1 2 3

R/A Ratio Pe rc e n ta g e

DISCUSSION

The present series “Study of QRS Duration and R/Q Ratio in the Assessment of

Severity of Acute Myocardial Infarction” was carried out on 75 patients admitted in

ICCU of Department of Medicine, Government Royapettah Hospital, Kilpauk Medical

College, Chennai-10.

For the study of “QRS Duration” in the severity of myocardial infarction (both

AWMI and IWMI) patients were divided into 3 groups.

Group A With QRS duration < 0.09 Sec.

Group B With QRS duration 0.09 - 0.11 see (intermediate QRS prolongation)

Group C With QRS duration > 0.11 see (Significant QRS prolongation)

For the study; patients of inferior wan myocardial infarction were divided into 3

groups according to “R/Q ratio” in lead II on 3rd day.

Group I Includes patients of IWMI with R/Q ratio> 2

Group II Includes patients of IWMI with R/Q ratio 1- 2

TYPE OF MYOCARDIAL INFARCTION

In the present study 44 patients (58.67%) were having inferior wall myocardial

infarction 28 patients (37.33%) were having anterior wall myocardial infarction and 3

(4.0%) were having both anterior and inferior wall myocardial infarction.

DISTRIBUTION OF EJECTION FRACTION

In the present study 34.61% of anterior wall myocardial infarction patients were

having LVEF of < 40% as compared to 17.07% of patients of inferior wall myocardial

infarction. The percentage of patients of anterior wall myocardial infarction with ejection

fraction of > 50% was only 15.38% as compared to 31.07% in inferior wall myocardial

infarction. So statistically significant lower ejection fraction in anterior wall myocardial

infarction as compared to IWMI (p< 0.001) was seen.

The observation was similar to that of Mark et al (1987) (53) who observed that

there is greater left ventricular involvement and dysfunction in patients with anterior

myocardial infarction of equivalent enzymatic size.

Eaton et al (1979) (54) in a limited series of 28 patients showed that anterior

infarcts are more at risk of expanding with thinning of the infarct zone combined with

acute regional dilatation than inferior infarcts. It is anticipated that this process would

lead to greater left ventricular regional wall motion abnormality both at rest and during

Strass et al (1980) (55) observed that there was greater involvement and reduced

function of the left ventricle in patients with anterior infarction compared to those with

inferior infarction of equivalent enzymatic size.

QRS DURATION AND DISTRIBUTION OF MYOCARDIAL INFARCTION:

In the present study most of the patients of inferior as well as anterior wall

myocardial infarction were distributed in group A (QRS < 0.09 sec.) 40% of AWMI

patients were having QRS duration > 0.09 seconds as compared to 30% of patients in

IWMI (p<0.05).

QRS DURATION AND ARRHYTHMIA IN MYOCARDIAL INFARCTION:

Ventricular ectopics were the most common arrhythmia observed in relationship

to QRS duration groups. Maximum incidence of ventricular tachycardia (44.44%) was in

group B (QRS 0.09-0.11 sec.). Out of the 8 patients in group C (QRS > 0.11 sec) 2

patients were (25.0%) having ventricular tachycardia as com pared to 3 patients (6.38%)

in group A (< 0.09 sec.) so statistically significant high incidence of malignant

arrhythmias was noted in patients of intermediate QRS prolongation (0.09 - 0.11 sec) and

significant QRS prolongation (> 0.11 see) in the present study.

Previous study by Pudil et al (2001) (38) showed that in hospital complication

including asystole, ventricular tachycardia, ventricular fibrillation, congestive heart

Prolonged QRS duration was a significant predictor of sustained monomorphic

VT inducibility (p<0.00l) (Relative risk 3.290, 95% confidence interval 2.185 to 4.953

for prolonged vs normal QRS duration) (44).

At multivariate analysis, only low left ventricular ejection fraction, prolonged

QRS duration, reduced heart rate variability index, and detection of approximately 2 runs

of unsustained VT per monitoring had an independent relation to late arrhythmic events

(45).

REGIONAL WALL MOTION ABNORMALITY AND EJECTION FRACTION IN

RELATION TO QRS DURATION:

In the present study akinesia was reported from 14 patients (87.5%) of group B

(0.09 - 0.11 sec.), 4 patients (66.67%) of group C (> 0.11 see) and 24 patients (50%) of

group A « 0.09 see); hypokinesia was reported from 2 patients (12.5%) of group B, 2

patients of group C (33.33%) and 22 patients (46.0%) of group A. Hence, regional wall

motion abnormality was having a significant relationship with QRS duration. Increased

QRS duration had an increased incidence of akinesia in the present study (p< 0.001).

In the present study patients with ejection fraction of >50% in group A was

35.42% in group C 16.67%. None of the patients in Group B was having ejection fraction

of> 50%.

In a previous study by Brilakis et al (46) QRS duration> 100 msec on standard 12

In 27 out of 28 postmyocardial patients in whom left ventricular systolic

dysfunction (defined as ejection fraction of < 40%) developed; QRS duration increased

from 107±12 milliseconds to128±18 milliseconds.

Pudil et al (2001) (38) showed that a QRS of <0.09 sec on admission

electrocardiogram is indicative of a relatively benign outcome compared with a QRS of

>0.09 sec. Patients with intermediate QRS prolongation (0.09 - 0.11 sec.) also associated

with decreased ejection fraction and increased incidence of akinesia. Hence intermediate

QRS duration prolongation had also statistically significant relationship with ejection

fraction and RWMA in a similar way to significant QRS prolongation (> 0.11 sec.).

QRS DURATION AND KILLIP CLASS:

In the present study in group A (< 0.09 sec.) 71.4% (n=35) of patients were

belonging to Killip class I as compared to 12.5% in group C. Patients with Killip class>

II were 4% in group A, 62.5% in group C and 16.6% in group B. These results are

statistically significant (p< 0.05).

In the present study mean QRS duration of class I patient was 0.08±0.01 as

compared to 0.10 in Killip class IV. As Killip class of patient increases mean QRS

duration also increases.

Above observations go in agreement with previous study by Brilakis et at (2002)

(46) in which patients with QRS duration < 100 milliseconds to be in Killip class II, III or

IV at presentation. Patients with QRS duration < 100 milliseconds, percentage of patients

with Killip class> II was 16.7% against 32% in patients with QRS duration > 100

Michaelides et al (1993) (42) reported that exercise induced QRS prolongation

was proportional to the number of coronary arteries with > 70% stenosis. Mean QRS

prolongation was 4.8±7.5 milliseconds in patients with I-vessel disease, 7.8±11.8

milliseconds in patients with 2-vessel disease and 13.3±12.1 milliseconds in patients with

3-vessel disease. Study by Brilakis. et al (2002) (46) showed increased QRS duration was

strongly associated with heart failure as evidenced by worse Killip class.

MORTALITY IN RELATION TO QRS DURATION:

In the present study, out of the 75 patients 6 (8.0%) expired. One from group A

(2.0%), 3 from group B (16.67%), and 2 (25.0%) from group C. In the mortality group,

except one patient of AWMI rest of them expired before echocardiography could be

done. So correlation with ejection fraction and R/Q ratio was not possible; hence

mortality was analysed on the basis of QR5 duration. Analysis of present study data

shows that increased QRS duration had a significant statistical relationship with mortality

(p< 0.05).

QRS duration measured on a standard ECG remains a powerful predictor of

mortality after adjustment for ejection fraction and other clinical covariates. Data in a

large population of post infarction patients indicates that QRS of 0.12 seconds is

associated with hazard ratio of 1.7; p = 0.001. Above observations in the present study

i.e; highest mortality 25% in group C patients (QRS > 0.11 sec.) is in agreement with the

observations of Fadl et al (2003). (47)

QRS duration remains a very powerful predictor of future cardiac events in post